Fibroblast growth factor 23 (FGF23) is a potent regulator of phosphorus (P) and vitamin D metabolism. Long-term dietary magnesium (Mg) deficiency increases circulating levels of FGF23, whereas the effects of short-term dietary Mg deficiency are unclear. Thus, the present study investigated whether short-term dietary Mg deficiency affects circulating levels of FGF23. We also assessed changes in renal mRNA expression of vitamin D metabolizing enzymes and type II sodium-phosphate (Na/Pi) cotransporters, since these are regulated by FGF23. Rats were fed a control diet (control group) or an Mg-deficient diet (Mg-deficient group) for 2, 4 or 7 days. Serum Mg levels were significantly lower in the Mg-deficient group than in the control group at all time points. Serum FGF23 levels were significantly higher in the Mg-deficient group than in the control group at day 7. The 25-hydroxyvitamin D-24-hydroxylase (24(OH)ase) mRNA levels were significantly higher in the Mg-deficient group than in the control group at day 7 . No significant differences in types IIa and IIc Na/Pi cotransporter mRNA levels were observed between the control and Mg-deficient groups. These results suggest that dietary Mg deficiency causes a rapid increase in circulating levels of FGF23 and renal 24(OH)ase mRNA levels.

We hypothesized that a zinc-deficient diet alters the mineral (calcium, magnesium, and phosphorus) components of bones, as well as hormones related to bone remodeling, and negatively affects bone metabolism. Four-week-old male Wistar rats were randomly assigned to one of three groups for 4 wk: a zinc-adequate group (C, 30 ppm); a zinc-deficient group (ZD, 1 ppm); and a pair-fed group (PF, 30 ppm), which was pair-fed to the ZD group. Bone mineral density and bone mechanical properties were reduced in the ZD group compared to the C and PF groups. Compared with the C and PF groups, serum osteocalcin, a bone formation marker, was reduced in the ZD group. Conversely, urine deoxypyridinoline, a bone resorption marker, was increased in the ZD group compared to the C and PF groups. Calcium and phosphorus concentrations in bone were not different among all groups. The bone magnesium concentration was significantly higher in the ZD group than in the PF and C groups. Interestingly, compared with the C and PF groups, the ZD group showed a reduction in serum calcium concentration along with an increase in serum parathyroid hormone (PTH) concentration. Although serum 1,25-dihydroxycholecalciferol concentration was significantly higher in the ZD and PF groups than in the C group, the rate of apparent calcium absorption was significantly lower in the ZD group than in the C and PF groups. Therefore, zinc deficiency is suspected to cause an increase in serum PTH concentration owing to an inability to maintain calcium homeostasis, resulting in bone fragility.

A magnesium (Mg)-deficient diet results in decreased serum phosphorus (P) levels and increased urinary P excretion; however, the mechanisms responsible for these effects are unclear. Fibroblast growth factor-23 (FGF-23) is a potent regulator of P homeostasis. To determine the mechanisms responsible for the change in serum levels and urinary excretion of P with Mg deficiency, the present study examined the effects of Mg deficiency on serum FGF-23 levels. Male rats were randomized by weight into two groups and fed a control diet (Mg concentration: 0.05%) or a Mg-deficient diet (Mg concentration: Mg-free) for 21 days. Serum P levels in rats fed the Mg-deficient diet were significantly lower than in rats fed the control diet. Furthermore, urinary P excretion was significantly higher in rats fed the Mg-deficient diet compared to rats fed the control diet. Conversely, the tubular reabsorption rate of P was significantly lower in rats fed the Mg-deficient diet than in the controls. Serum FGF-23 levels in rats fed the Mg-deficient diet were significantly higher than those in animals fed the control diet. The results from the present study indicate that 1) Mg deficiency increases serum FGF-23 levels; and 2) Mg deficiency causes increased urinary P excretion via inhibition of renal P reabsorption, resulting in a lowering of serum P levels. Moreover, we suggest that the high serum FGF-23 levels induced by Mg deficiency contribute to the decrease in renal P reabsorption.

A magnesium (Mg) deficiency induces changes in calcium (Ca) and phosphorus (P) metabolism; however, the mechanisms responsible for these effects remain unclear. Since 1,25-dihydroxyvitamin D3 and type II sodium-phosphate (Na/Pi) cotransporters are essential regulators of Ca and P metabolism, this study examined the effects of Mg deficiency on the mRNA expression of vitamin D metabolizing enzymes (25-hydroxyvitamin D-1α-hydroxylase (1α(OH)ase) and 25-hydroxyvitamin D-24-hydroxylase (24(OH)ase)), and Na/Pi cotransporters (type IIa and IIc) in the rat kidney. Rats were divided into two groups and fed a control diet (Mg concentration: 0.05%) or a Mg-deficient diet (Mg concentration: Mg-free) for 21 days. 1α(OH)ase mRNA levels were significantly decreased in rats fed the Mg-deficient diet, while 24(OH)ase mRNA levels were significantly increased, compared to rats fed the control diet. Type IIa and IIc Na/Pi cotransporter mRNA levels in rats fed the Mg-deficient diet were significantly decreased compared to rats fed the control diet. These results suggest that Mg deficiency induces downregulation of 1α(OH)ase and type IIa and IIc Na/Pi cotransporters, and upregulation of 24(OH)ase in the kidney.

In order to clarify the effects of a high-calcium (Ca) diet on bone formation in magnesium (Mg)-deficient rats, this study focused on the effects of a high-Ca diet on serum insulin-like growth factor-1 (IGF-1) levels. Male rats were randomized by weight into four groups, and fed one of four experimental diets containing two different Mg concentrations (0.05% (normal-Mg) or Mg-free (Mg-deficient)), and two different Ca concentrations (0.5% (normal-Ca) or 1.0% (high-Ca)) for 14 days. Serum concentrations of osteocalcin and IGF-1 were significantly lower in rats fed the Mg-deficient diet than in rats fed the normal-Mg diet. On the other hand, dietary Ca concentration had no significant influence on serum concentrations of osteocalcin and IGF-1. This study suggested that: 1) a high-Ca diet has no preventive effects on the decreased bone formation seen in Mg-deficient rats; and 2) a high-Ca diet does not enhance serum IGF-1 levels in Mg-deficient rats. Moreover, unchanged serum IGF-1 concentrations may contribute to the decreased bone formation seen in Mg-deficient rats receiving a high-Ca diet.

therapy 53 Adverse events 455 -reactions 455 AIDS 332 Allograft rupture 71 Alloimmune hemolysis 473 Ammonium chloride 74 Amyloidosis 68 Anemia 27, 89 Angiotensin II 373 Angiotensin-converting enzyme inhibitors 149, 268 Anion gap 369 Ankle-arm blood pressure index 107 Anticardiolipin antibodies 351 Antilactoferrin antibody 57 Antineutrophil cytoplasmic antibody 57 Antiretroviral therapy 332 Aorto-iliac atherosclerosis 487 Arterial blood gas values 319 Aspergillus 329 AST-120 232 Atheroembolization 263 Atherosclerosis 107, 487 Axillo-femoral bypass 487 Basement membrane 175 Behçet disease 68, 217 Bidialysis 429 Big men 429 Bioelectrical impedance analysis 311 Biological markers 48 Blood pressure 193 Body mass index 169 Bone markers 283 -turnover

高濃度の食餌性リンを投与したラットにおける副甲状腺ホルモンの脱感作について検討を行ったところ, 血清中PTH濃度の上昇が観察されたにも関わらず, 血清中1α, 25 (OH) 2D3濃度の変化は観察されず, また尿中cAMP排泄量は有意に低値を示した。これは高リン食投与により分泌が維持されたPTHの作用が果たされずPTHの脱感作が観察された。また, PTHの作用部位であるPTH/PTHrP受容体mRNAが低下しており, 翻訳後のPTH/PTHrP受容体の量が減少していることが推察でき, PTHの脱感作が起きていることが推察された。